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Role of selenium against lead toxicity in male rats
Author(s) -
Othman Azza I.,
El Missiry Mohammed A.
Publication year - 1998
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/(sici)1099-0461(1998)12:6<345::aid-jbt4>3.0.co;2-v
Subject(s) - lead acetate , chemistry , lipid peroxidation , glutathione , glutathione reductase , selenium , superoxide dismutase , toxicity , antioxidant , medicine , endocrinology , kidney , alkaline phosphatase , glutathione peroxidase , pharmacology , biochemistry , enzyme , biology , organic chemistry
Male albino rats were intramuscularly administered a single dose of lead acetate (100 μmol/kg b.wt). Another group of rats were injected with sodium selenite (10 μmol/kg b.wt) before lead intoxication. After 3 and 24 hours, lead treatment resulted in significant increases in acid and alkaline phosphatases, GOT and GPT, total proteins, and cholesterol in serum. The total triglycerides in serum was decreased after 24 hours of intoxication. Lead treatment also produced significant elevation of lipid peroxidation in liver and kidney. The antioxidant capacity of hepatic and renal cells in terms of the activities of superoxide dismutase, glutathione reductase, and glutathione content was diminished. It appears from these results that lead may exert its toxic effect via peroxidative damage to renal and hepatic cell membranes after 24 hours. Selenium administration prior to lead injection produced pronounced prophylactic action against lead effects, and it is observed that selenium enhances the endogenous antioxidant capacity of the cells by increasing the activities of the superoxide dismutase and glutathione reductase and the glutathione content. As a result, the lipid peroxidation was decreased in both liver and kidney. © 1998 John Wiley & Sons, Inc. J Biochem Mol Toxicol 12: 345–349, 1998